CST, 4999S, Phospho-RelB (Ser552) Antibody

Polyclonal Antibody for studying RelB (Ser573) phosphate. Validated for WB,IP,IF,F. Highly specific and rigorously validated in-house, Phospho-RelB (Ser552) Antibody (CST #4999) is ready to ship. Product Usage Information Western Blotting: 1:1000 Immunoprecipitation: 1:100 Immunofluorescence (Immunocytochemistry): 1:100 Flow Cytometry (Fixed/Permeabilized): 1:400 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at -20°C. Do not aliquot the antibody. Protocol Available protocols: Western Blotting, Immunoprecipitation, Immunofluorescence (Immunocytochemistry), Flow Cytometry (Fixed/Permeabilized) Specificity / Sensitivity Phospho-RelB (Ser552) Antibody detects endogenous levels of RelB only when phosphorylated at Ser552. Species Reactivity: Human, Mouse Source / Purification Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser552 of mouse RelB. Antibodies are purified by protein A and peptide affinity chromatography. Background Transcription factors of the nuclear factor κB (NF-κB)/Rel family play a pivotal role in inflammatory and immune responses (1,2). There are five family members in mammals: RelA, c-Rel, RelB, NF-κB1 (p105/p50), and NF-κB2 (p100/p52). Both p105 and p100 are proteolytically processed by the proteasome to produce p50 and p52, respectively. Rel proteins bind p50 and p52 to form dimeric complexes that bind DNA and regulate transcription. In unstimulated cells, NF-κB is sequestered in the cytoplasm by IκB inhibitory proteins (3-5). NF-κB-activating agents can induce the phosphorylation of IκB proteins, targeting them for rapid degradation through the ubiquitin-proteasome pathway and releasing NF-κB to enter the nucleus where it regulates gene expression (6-8). NIK and IKKα (IKK1) regulate the phosphorylation and processing of NF-κB2 (p100) to produce p52, which translocates to the nucleus (9-11). RelB, which is generally activated by non-canonical signaling, forms heterodimers with either p50 or p52 NF-κB subunits to regulate transcription (12,13). RelB null mice are significantly impaired in inflammatory responses and hematopoietic differentiation (14,15). Phosphorlyation at Thr84 and Ser552 results in proteosomal degradation (16). Alternate Names I-Rel; IMD53; IREL; REL-B; RELB; RELB proto-oncogene, NF-kB subunit; Transcription factor RelB; v-rel avian reticuloendotheliosis viral oncogene homolog B (nuclear factor of kappa light polypeptide gene enhancer in B-cells 3); v-rel reticuloendotheliosis viral oncogene homolog B; v-rel reticuloendotheliosis viral oncogene homolog B, nuclear factor of kappa light polypeptide gene enhancer in B-cells 3 Specification REACTIVITY: H M SENSITIVITY: Endogenous MW (kDa): 70 SOURCE: Rabbit